Jakab F, Sugár I, Ráth Z, Nágy P, Faller J
Department of Surgery, Semmelweis University of Medicine, Budapest, Hungary.
HPB Surg. 1996;10(1):21-6. doi: 10.1155/1996/90536.
The relationship between the changes in portal venous and hepatic arterial blood flows, in the liver is a much disputed question, it has tremendous significance in the practice of transplantation, and an explanation has been available since 1981, when Lautt published the so-called "adenosine washout theory". According to our earlier observations the decrease of portal pressure or flow consistently led to an increase in hepatic artery flow. At the same time changes in hepatic artery flow or pressure seemed to produce only inconsistent effects on the portal circulation. In the present experiments liver transplantation (OLTX) was carried out on mongrel dogs by Starzl's method. Electromagnetic flow probes were placed on the hepatic artery and the portal vein before removal of recipient's liver, and after completion of all vascular anastomoses to the newly inserted liver, during the recirculatory phase of OLTX. The flow probes were connected to a Hellige electromagnetic flowmeter, portal venous and systemic arterial pressures were also recorded. The control HAF was 241 +/- 23 ml/min, the average PVF was 517 +/- 47 ml/min before removal of the recipient's liver. In the recirculatory phase of HAF increased, by 71 +/- 12% (p < 0.001). The PVF decreased in most animals after OLTX. The decrease was in average -40.2 +/- 3.5% (p < 0.001). The THBF calculated by adding the HAF and PVF showed a small, but not significant decrease recirculation. The systemic arterial pressure decreased slightly and portal vein pressure rose in most animals after OLTX. There was a substantial increase in portal inflow resistance and prehepatic arteriolar resistance and a decrease in hepatic artery resistance. The decrease of PVF after OLTX can be explained by progressive fluid accumulation in the liver parenchyma and increased sinusoidal and portal inflow resistance. The prolonged and continuous increase in hepatic artery flow during the recirculatory phase of OLTX may be due to the decrease of portal flow. The exact mechanism, by which a change in portal flow leads to arteriolar dilatation, can be most probably explained by the "adenosine washout theory" of Lautt.
门静脉血流变化与肝动脉血流变化在肝脏中的关系是一个备受争议的问题，它在移植实践中具有重大意义，自1981年劳特发表所谓的“腺苷洗脱理论”以来，就有了一种解释。根据我们早期的观察，门静脉压力或血流量的降低始终会导致肝动脉血流量增加。与此同时，肝动脉血流量或压力的变化似乎对门静脉循环仅产生不一致的影响。在本实验中，采用施塔兹的方法对杂种犬进行原位肝移植（OLTX）。在切除受体肝脏前，以及在OLTX再循环阶段完成所有与新植入肝脏的血管吻合后，将电磁流量探头置于肝动脉和门静脉上。流量探头连接到海利格电磁流量计，同时记录门静脉和体动脉压力。在切除受体肝脏前，对照肝动脉血流量为241±23毫升/分钟，平均门静脉血流量为517±47毫升/分钟。在再循环阶段，肝动脉血流量增加了71±12%（p<0.001）。大多数动物在OLTX后门静脉血流量下降。平均下降-40.2±3.5%（p<0.001）。通过将肝动脉血流量和门静脉血流量相加计算得出的总肝血流量在再循环时出现了轻微但不显著的下降。大多数动物在OLTX后体动脉压力略有下降，门静脉压力升高。门静脉流入阻力和肝前小动脉阻力大幅增加，肝动脉阻力降低。OLTX后门静脉血流量的下降可以用肝实质中液体的逐渐积聚以及肝血窦和门静脉流入阻力增加来解释。在OLTX再循环阶段肝动脉血流量的持续长时间增加可能是由于门静脉血流量的减少。门静脉血流变化导致小动脉扩张的确切机制很可能可以用劳特的“腺苷洗脱理论”来解释。
